Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Blood & Lymph > Antiplatelets, Anticoagulants & Thrombolytics 1 > Flashcards

Antiplatelets, Anticoagulants & Thrombolytics 1 Flashcards

1
Q

3 classes of drugs that keep platelets in control

A
  1. Anti-platelet
  2. Anti-coagulant
  3. Fibrinolysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Which polymorphisms must you be aware of in platelet drugs (2)?

A
  1. warfarin
  2. clopidogrel
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Where do platelet clotting factors assemble?

A

On the surface of platelets → change shape to spiny structure increasing surface area & charge. This helps the factors assemble and expose phosphatidyl C ring → Ca2+ binds surface & clotting factors

(w/o activation → no clotting)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Aspirin MOA

A

Irreversible inhibition of COX-1 & COX-2 → suppress thromboxanes & prostaglandins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How does Aspirin inhibit COX enzymes

A

attaches acetyl group → steric hindrance → cannot come into contact w/arachidonic acid → no Thromboxane A2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Aspirin indications (2)

A
  1. TIA
  2. Acute coronary syndrome (NSTEMI or STEMI MI)

(fever, pain & headache)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Aspirin contraindications (5)

A
  1. GI ulcer
  2. Hx of asthma
  3. Children: chicken pox of flu → reye’s syndrome
  4. Combo w/methotrexate
  5. Last trimester of pregnancy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Why can aspirin not be used w/methotrexate (15 mg/week)?

A

reduces methotrexate elimination → decreases renal clearance & displaces it from protein binding sites → hematologic toxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Why is aspirin not given to women in the 3rd trimester of pregnancy?

A

acetylation of fetal enzymes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How does aspirin cause GI bleeding?

A

blocking prostaglandin synthesis → decreased renewal of epithelium cells → decreased mucus production & protection of the stomach lining.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Aspirin Adverse Effects (7)

A
  1. Hemolytic anemia
  2. Bleeding: GU, gingiva
  3. GI inflammation, heartburn
  4. Asthma, anaphylaxis, nasal congestion
  5. Mental confusion, drowsiness
  6. Tinnitis, hearing loss
  7. Dizzy, vertigo
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Hemolytic anemia may occur when ______ patients are given aspirin

A

G6PD deficient

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

At low dose, aspirin _____ (increases/decreases) gout attack; high dose ______ (increases/decreases) the risk of gout attack.

A
  • increases
  • decreases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

P2Y12 receptor antagonist MOA: stops GPIIb/IIIa activation → decreases platelet aggregation by ______ (2).

A
  1. decreases Ca release
  2. increases cAMP levels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Clopidogrel MOA

A
  1. prodrug metabolized by CYP2C19
  2. Irreversible blocks ADP receptor on platelets (lasts 7 days; life of platelet)

(dose-dependent; metabolized by CYP450)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Clopidogrel drug interactions (3)

A
  1. CYP2C19 inhibitors (omeprazole or Esomeprazole)
  2. Opioids
  3. Repaglinide

(may need to genotype your patient first)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Prasugrel is a prodrug, like clopidogrel, and is converted to active metabolite by _____ (2) enzymes. It irreversibly inhibits ______.

A
  • CYP3A4, CYP2B6
  • P2Y12

(indicated for acute coronary syndrome)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Prasugrel contraindications (2)

A
  1. pathological bleeding
  2. Hx TIA/stroke
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Which 2 P2Y12 antagonists are reversible inhibitors?

A
  1. ticagrelor (also p-glycoprotein inhibitor)
  2. Cangrelor

(clopidogrel & prasugrel are irreversible inhibitors)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Which is the only antiplatelet drug that is NOT given orally?

A

Cangrelor (IV)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Why would you give cangrelor instead of another P2Y12 antagonist?

A

hepatic disease; this drug is not metabolized by the liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How do GP2b/3a inhibitors work?

A

prevents fibrinogen from binding and bringing platelets together

23
Q

GP2b/3a inhibitors

A
  1. Abciximab
  2. Eptifibatide
24
Q

Abciximab is intended for use with _______ (2)

A
  1. aspirin
  2. heparin

(for coronary intervention)

25
Q

Abciximab is a chimeric human-murine monoclonal ab against glycoprotein 2b/3a receptor of platelets. It is produced by _______.

A

continuous perfusion in mammalian cells

26
Q

Abciximab onset?

Platelet recovery?

A
  1. rapid: half-life < 10 min
  2. platelet recovery w/in 48 hours
27
Q

Thrombin inhibitors bind to ______. Why is this receptor unique?

A
  • PAR1
  • Carriers its own ligand (it just needs enzyme to cleave it → activation)
28
Q

Vorapaxar is indicated for patients w/______.

A

hx of MI or peripheral artery disease

29
Q

Vorapaxar MOA

A

thrombin inhibitor: reversible antagonist of PAR-1 (protease-activated receptor-1)

(long half life: 4 weeks!)

30
Q

Cilostazol indicated to reduce _______

A

symptoms of intermittent claudication

31
Q

Cilostazol MOA

A

inhibits phosphodiesterase III activity → inhibits platelet aggregation & vasodilation

32
Q

Cilostazol contraindications

A

heart failure

33
Q

Cilostazol: AE

A
  1. tachycardia, palpitations
  2. thrombocytopenia
  3. leukopenia
34
Q

What is the major targets of coagulation inhibition (2)?

A
  1. Prevention of Thrombin IIa formation (inhibiting Xa)
  2. second most effective is factor X
35
Q

INR measures _____

A

warfarin activity

(PT monitors this as well)

36
Q

Normal prothrombin time

A

11-15 seconds

(prolonged in patients on warfarin; may double)

37
Q

INR =

A

PT patient/ PT normal)ISIS

(ISI determined by manufacturer of thromboplastin reagent)

38
Q

Typical INR range

A

1.1

39
Q

INR range of _____is an effective therapeutic range for warfarin

A

2-3

40
Q

aPTT (activated partial thromboplastin time) uses (2)

A
  1. heparin activity
  2. investigate bleeding disorders
41
Q

Normal PTT

A

35 seconds

42
Q

How is [heparin] measured?

A

Anti-Xa activity

43
Q

Which 2 classes of drugs are Direct/Novel Oral Anticoagulants (DOAC/NOAC)?

A
  1. Factor Xa inhibitors
  2. Thrombin (Factor IIa) inhibitors
44
Q

List the factor Xa inhibitors (4)

A
  1. Apixaban
  2. Rivaroxaban
  3. Edoxaban
  4. Betrixaban

(the -“xaban”s)

45
Q

List the thrombin (factor IIa) inhibitor

A

Dabigatran

46
Q

RivaroXAban reduces the risk of _______ & treats ______ (2).

A
  1. stroke, systemic embolism in nonvalvular a-fib
  2. DVT, pulmonary embolism
47
Q

Patients with a renal clearance < ______mL/min should not use RivaroXAban. Why?

A
  • 15
  • excretion is mainly via tubular & glomerular filtration
48
Q

RivaroXAban discontinuation may increase risk of ______

A

stroke in nonvalvular a-fib

(Dabigatran also increases risk of thrombotic events if d/c early)

49
Q

ApiXAban recommended dosage

A

5 mg 2xs/daily

50
Q

ApiXAban contraindications (2)

A
  1. Pregnancy & Lactation
  2. Severe hepatic impairment
51
Q

ApiXAban should NOT be used with ______ (Rx)

A

ELIQUIS

(P-gp & strong CYP3A4 inhibitors also)

52
Q

ApiXAban BetriXAban & EdoXAban inhibit _____(2).

A
  1. free & clot-bound FXa
  2. prothrombinase activity
53
Q

EdoXaban reduces risk of _____

A

stroke & PE in patients w/nonvalvular a-fib

Blood & Lymph (29 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions